RESUMEN
Presuming that Alzheimer's disease (AD) might represent an antagonistic pleiotropic phenomenon derived from the evolvability of multiple amyloidogenic proteins, targeting such proteins simultaneously could enhance therapeutic efficacy. Furthermore, considering that amyloid-ß (Aß) immunotherapies during reproductive life stage might adversely decrease Aß evolvability in an offspring's brain, the disease-modifying Aß immunotherapies should be limited to post-reproductive time in lifespan. Thus, current Aß immunotherapy strategies should be revised accordingly. Given that the "adiponectin paradox" might underlie both amyloidosis and cognitive dysfunction in aging brain, blocking activin signaling situated downstream of the adiponectin paradox might be an alternative strategy to prevent AD.